Sleep Interval Research Articles

Effects of Early and Late Nocturnal Sleep on Declarative and Procedural Memory

Recall of paired-associate lists (declarative memory) and mirror-tracing skills (procedural memory) was assessed after retention intervals defined over early and late nocturnal sleep. In addition, effects of sleep on recall were compared with those of early and late retention intervals filled with wakefulness. Twenty healthy men served as subjects. Saliva cortisol concentrations were determined before and after the retention intervals to determine pituitary-adrenal secretory activity. Sleep was determined somnopolygraphically. Sleep generally enhanced recall when compared with the effects of corresponding retention intervals of wakefulness. The benefit from sleep on recall depended on the phase of sleep and on the type of memory: Recall of paired-associate lists improved more during early sleep, and recall of mirror-tracing skills improved more during late sleep. The effects may reflect different influences of slow wave sleep (SWS) and rapid eye movement (REM) sleep since time in SWS was 5 times longer during the early than late sleep retention interval, and time in REM sleep was twice as long during late than early sleep (p < 0.005). Changes in cortisol concentrations, which independently of sleep and wakefulness were lower during early retention intervals than late ones, cannot account for the effects of sleep on memory. The experiments for the first time dissociate specific effects of early and late sleep on two principal types of memory, declarative and procedural, in humans.

The Relationship Between Sleep Deprivation and the Nocturnal Decline of Blood Pressure

Blood pressure (BP) has a circadian pattern with a 10% to 15% drop in systolic and diastolic BP comparing nighttime and daytime averages. The mechanism and the "reason" for the decline of nocturnal blood pressure has not been described. If the nocturnal decline is a restorative physiologic process we reasoned that sleep deprivation would increase the nocturnal drop. Thus, we tested the hypothesis that there is a compensatory decline in nocturnal sleep blood pressure after a period of nocturnal sleep deprivation. Twenty-four house staff personnel (normotensive and not taking any BP medications) with a mean age of 29.3 years were recruited for this study (13 men and 11 women). Subjects were randomly assigned to have 24-h BP monitoring after being sleep deprived (on call with 3 +/- 1.3 h of sleep) or after a normal night's sleep (7.3 +/- 0.8 h). There was no significant difference in hours asleep or time to bed or time awake for both 24-h studies. Subjects had similar activities for both monitoring intervals. The percent change in day awake versus night asleep mean values for systolic BP, diastolic BP, and mean arterial pressure for sleep deprived and normal night's sleep intervals were compared using paired t tests. None of these paired parameters were significantly different despite a subjectively "deeper" sleep postcall. In conclusion, sleep deprivation does not appear to result in a compensatory decline in nocturnal blood pressure. Thus, the "reason" for the normal nocturnal decline in blood pressure remains to be explored.

Sleep patterns in women after coronary artery bypass surgery

Sleep patterns were examined over a 6-month time period after coronary artery bypass graft surgery (CABG) using a wrist-worn actigraph and the Sleep-Rest subscale of the Sickness Impact Profile. The sample included 22 women during the first postoperative week (T1), and 13 of these women during the first posthospitalization week (T2) and the sixth (T3) and twenty-fourth postoperative weeks (T4). Nighttime sleep became less fragmented and, over time, total sleep became more consolidated during nighttime hours, as shown by significant decreases in day, evening, and total sleep and increases in the percentage of total sleep occurring at night during T1. There were also increases in nighttime sleep and percentages of total sleep and the mean sleep interval and decreases in day sleep and evening sleep and nighttime awakenings during T1 through T4. Decreases in the Sleep-Rest subscale indicated perceived improvement in sleep consistent with changes in objective sleep measures over 6 months. These data can be used to help women anticipate changes in sleep patterns over the course of recovery. They suggest the importance of interventions to improve sleep during hospitalization and posthospitalization recovery.

The effect of sleep intervals on analysis of 24-h ambulatory blood pressure data

Twenty-four hour blood pressure exposure and circadian blood pressure variability may be important predictors of hypertensive end-organ damage. Since sleep is a major determinant of circadian blood pressure decline, day/night blood pressure changes may be affected by sleep intervals. The current study compares 24-h blood pressure results with and without adjustment for patient-specific sleep intervals. Forty male hypertensive patients (22 with renal insufficiency and 18 with normal renal function) underwent 24-h blood pressure study with SpaceLabs 90207 monitors. They also filled out sleep questionnaires to evaluate time awake and asleep during the day and night intervals. Data was analyzed with and without adjustment for daytime asleep and nighttime awake intervals. The percent change in systolic, diastolic, and mean arterial pressure as well as heart rate was not different statistically or clinically with or without adjustment for sleep intervals. Nevertheless, there was a progressive increase in the day versus night percent change in these hemodynamic parameters with adjustment for sleep intervals. When we used arbitrary cut-offs to define "non-dipper", ie, less than 10% drop in a given hemodynamic parameter, and used patient-specific sleep intervals, clinically and statistically different numbers of "non-dippers" were seen versus sleep unadjusted data (19 v 12, using diastolic BP, P < .01). In conclusion, it may not be necessary to adjust for sleep intervals when relating 24-h blood pressure and day/night blood pressure variability to hypertensive end-organ damage. However, arbitrary cut-offs to define "non-dippers" may be greatly and capriciously affected by sleep/awake intervals.(ABSTRACT TRUNCATED AT 250 WORDS)

Dependence on REM sleep of overnight improvement of a perceptual skill.

Several paradigms of perceptual learning suggest that practice can trigger long-term, experience-dependent changes in the adult visual system of humans. As shown here, performance of a basic visual discrimination task improved after a normal night's sleep. Selective disruption of rapid eye movement (REM) sleep resulted in no performance gain during a comparable sleep interval, although non-REM slow-wave sleep disruption did not affect improvement. On the other hand, deprivation of REM sleep had no detrimental effects on the performance of a similar, but previously learned, task. These results indicate that a process of human memory consolidation, active during sleep, is strongly dependent on REM sleep.

Effects of diurnal sleep on secretion of cortisol, luteinizing hormone, and growth hormone in man.

Evidence has been provided for an influence of nocturnal sleep on the secretion of cortisol, LH, and GH in man. Although nocturnal sleep inhibits cortisol secretion during the first hours, it augments the secretion of LH and GH. To separate the effects of circadian rhythm from those of sleep, the present experiments examined the influence of diurnal sleep on the release of cortisol, LH, and GH in 12 young men. Subjects slept on 2 different occasions. After a night of wakefulness, subjects were assigned to bed at 0800 h the following morning. Lights were turned off either at 1100 or 1500 h to enable sleep. Effects of diurnal sleep were evaluated by comparing blood hormone concentrations during the interval from 1100-1500 h between subjects when sleeping and awake. Comparing hormonal concentrations during the 4 h of sleep after 1100 h with those during the 4-h sleep interval after 1500 h provided evidence for an influence of circadian rhythm on cortisol and LH release. Diurnal sleep, as has been shown for nocturnal sleep, augmented the secretion of LH and GH. However, in contrast to nocturnal sleep, diurnal sleep failed to suppress cortisol release, suggesting that sleep does not inhibit cortisol release at any point of its circadian rhythm, but only within a limited range of entrainment.

Sleep Deprivation and Resident Performance

Cognitive and complex motor performance may be impaired by extended sleep deprivation, but objective data concerning the effects in residents of the sleep deprivation engendered by usual hospital on-call schedules are scant and conflicting. We studied three cohorts of surgical residents (N = 26) who were on call every other night. Each resident kept a sleep diary, gave a self-assessment of motivation and fatigue, and underwent a battery of psychometric tests each morning for 18 or 19 days. The psychometric tests measured cognition, discernment, visual and auditory vigilance, and rapid eye-hand coordination. Sleep deprivation was defined as the lack of four hours of continuous sleep during the preceding 24 hours, and it occurred during 89% of the on-call nights. Daily testing in a repeated-measures design allowed each participant to serve as his or her own control. Sleep deprivation did not affect overall cognitive or motor performance. Further analysis of the correlation between sleep parameters (total sleep and longest uninterrupted sleep interval) and performance on each component of the psychometric test battery identified changes in performance on some tests but only trivial effects due to sleep. The assumption that sleep deprivation associated with usual on-call schedules impairs cognitive and motor performance of residents such that clinical care of patients may be compromised is not supported by our observations.

Perception of waking and sleeping: possible implications for the evaluation of insomnia.

Perception of awakening, its connection to electroencephalogram (EEG), and its significance for morning recall were studied in insomniacs and normals. Fourteen insomniacs and 14 age- and sex-matched controls kept a sleep log for 1 week and slept once in the laboratory (standard polygraphy). In addition, actual perception of awakening was measured by a behavioral device. Results suggest that physiological arousal is necessary, but not sufficient, for perception of awakening. Many arousals that are not perceived occur during the first REM-NREM cycle. Insomniacs nearly exclusively perceive those arousals occurring after consolidated sleep (at least 15 min) and at the beginning of interrupted sleep intervals. It is suggested that insomniacs perceive these intervals as continuous wakefulness and have difficulty in perceiving short-lasting sleep, whereas controls often do not perceive wakefulness at all. The latter may be a sleep-protecting mechanism. Number and correlation suggest that recalled awakenings are exactly those perceived. The connection between physiological and experimental subjective data is discussed.

Home pneumograms in normal infants

To obtain age-specific normative data, we performed home cardiorespiratory recordings (pneumograms) in 56 normal infants at 1 month of age. A repeat pneumogram was performed at 3 months in 39 infants. Total sleep time was determined and all sleep intervals were summed and analyzed for five respiratory pattern variables: frequency of all apneic episodes greater than or equal to 6 seconds in duration (A6/D%), periodic breathing, longest apneic episode, and number of episodes greater than 11 and greater than 15 seconds. The normal infants at 1 and at 3 months were compared with 66 patients with apnea of infancy. Median A6/D% was 0.1 in the normal infants at 1 and 3 months, compared with 0.64 in those with apnea of infancy (P less than 0.001). Median periodic breathing was 0.4 and 0.2 episodes per 100 minutes in the normal infants at 1 and 3 months, respectively, compared with 1.25 in infants with apnea of infancy (P less than 0.001). Median longest apneic episode was 8.0 seconds in the normal infants at 1 and 3 months, compared with 11 seconds in those with apnea of infancy (P less than 0.001). No normal infant had an apneic episode greater than 15 seconds in duration, whereas the group with apnea of infancy had 0.4 +/- 1.0 episodes of apnea of greater than 15 seconds (P less than 0.01). Despite these significant group differences, use of these respiratory patterns either alone or in combination permitted only about 80% correct classification of normal infants and those with apnea of infancy.

Pharmacokinetics of a sustained-release theophylline preparation in infants and preschool children with asthma

Sustained-release theophylline formulations should be most useful in young children who have rapid clearance and long sleep intervals. Somophyllin-12 is a recently introduced, newly designed, bead-filled capsule. We tested its ability to provide adequate serum concentrations at steady state in 16 children ages 0.9 to 5.1 yr. On a 12 hourly dosing schedule, mean dose was 25.9 mg/kg per day, and mean fluctuation was 138%. Seven children (43.8%) had fluctuations less than 100%, whereas four children (25%) had fluctuations more than 200%. Six patients with excessive fluctuation (>100%) were restudied on an eight hourly dosing schedule. Mean dose was 28.7 mg/kg per day, and fluctuation was 59%. Because of the excessive fluctuation (>100%) experienced by half these young children, therapy with this product should be initiated with an eight hourly dosing schedule. However, when dose and dosing interval are subsequently individualized, many young children can be switched to twice daily dosing with its improved compliance and convenience.

CARDIOVASCULAR RESPONSE TO HYPOXIA IN PUPPIES DURING NATURAL SLEEP

To examine the maturation of the cardiovascular response to hypoxia (FiO2=.15) during natural sleep, we studied 48 chronically instrumented unanesthetized beagle puppies at 15 and 30 days of age. We measured the RR interval and mean aortic blood pressure (MAP). In addition, in a subset of 10 puppies, we measured cardiac output (CO) by the Fick principle. After baseline measurements, puppies were exposed to hypoxia for 1-2 hrs. During normoxia, at 15 days of age: MAP was lower (mean 10%, p<.025) and CO higher (mean 20%,p<.05) in REM than in quiet sleep. There was no difference in RR interval between the 2 sleep states. In the older puppies, similar results were obtained except that there was no difference in CO between REM and quiet sleep. In response to hypoxia at 15 days of age, there was a decrease in CO (mean 30%,p<.05), an increase in MAP (mean 8%,p<.025) and no change in RR interval during REM sleep. In quiet sleep, MAP and RR interval did not change; CO could not be accurately measured as periods were usually less than 3 min. in duration. In the older puppies, hypoxia induced a decrease in CO in both sleep states (mean 30%,p<.025), a decrease in RR interval in quiet sleep and an increase in MAP during REM sleep. We conclude that in puppies: 1) CO is dependent on sleep state during normoxia at 15 but not at 30 days of age; with hypoxia, CO is reduced in both sleep states; 2) systemic vascular resistance is lower in REM sleep when compared to quiet sleep in normoxia and increases with hypoxia in both sleep states and 3) stroke volume is smaller in quiet than in REM sleep in normoxia and decreases with hypoxia in both sleep states.

Acute heroin abstinence in man: II. Alterations in rapid eye movement (REM) sleep

The purpose of this study was to examine the effects of withdrawal from heroin upon rapid eye movement (REM) sleep. Subjects included both heroin-dependent patients and drug-free controls. The drug users were young males who had an average daily intake of approximately 973 mg of 92–98% pure heroin before entering the study. All electrophysiological data were obtained via a telemetry system on a 24-hour per day basis for 5 to 7 consecutive days. EEC records were scored into the standard awake and sleep states. Results showed a marked decrease in total amount of REM sleep during heroin withdrawal. This total decrease was associated with a decrease in duration of individual REM episodes and a large decrease in the number of occurrences of REM sleep. The heroin-dependent patients during withdrawal also showed a prolonged latency from sleep onset to first REM episode and a reduced number of REM shifts per 24-hour period. No significant difference in REM sleep interval was observed between the control subjects and drug users. Some of the overt behavioral characteristics associated with heroin withdrawal may be indirectly related to the concurrent loss in REM sleep as observed in this study.

Perception of the duration of sleep intervals as a function of EEG sleep stage

Subjects were able to estimate with relative accuracy the durations of sleep intervals made up predominantly of EEG stage 1-REM but not of delta. Successful estimation required recall of a stimulus marking the beginning of an interval, but did not depend on time awake or on the EEG stage just prior to awakening. These results are consistent with the proposition that the passage of time is registered as part of the ongoing mentation of REM sleep. Correlation of time estimates with elapsed time for REM periods but not for delta periods makes comparison of the mean time estimates for these two conditions equivocal.

Sleep-stage regulation of ventricular arrhythmias in the unanesthetized pig.

In two groups of purebred juvenile Hampshire pigs, left anterior descending coronary occluders were implanted. The pigs were then adapted to the recording chamber until they would manifest a criterion pattern of sleep while in it. In group A, permanent coronary artery occlusions were produced, and the effects of various sleep stages on the resultant cardiac arrhythmias were observed. Sleep intervals during which transitional and slow wave (SW) sleep alternated were correlated with increased arrhythmias relative to the awake state (P less than 0.04). The increase was maximum during sustained periods of SW sleep. Intervals during which rapid eye movement (REM) sleep predominated were correlated with a reduction in arrhythmias. In group B, temporary occlusions were made during both an awake condition and after criterion patterns of either SW or REM sleep. Occlusions after SW sleep reduced the ventricular fibrillation latency compared with that during the awake control state (P less than 0.05), whereas occlusions after REM sleep increased ventricular fibrillation latency (P less than 0.05). We conclude that SW SLEEP, BUT NOT REM sleep, has a deleterious effect on the ischemic myocardium. REM sleep may have a beneficial effect, since it increases ventricular fibrillation latency. Heart rate changes do not appear to be correlated with the effects of either sleep stage.

Nocturnal sleep in rhesus monkeys

In 71 nocturnal sleep recordings of ten juvenile rhesus monkeys, a cyclic pattern of alternating Awake, nonREMP sleep and REMP (rapid eye movement period) was demonstrated. Sleep occurred at an average of 80% of the recording periods and REMP occupied 15% of the sleep time. The average duration of the REMP episodes was 6 min and they occurred cyclically every 51 min throughout the night. A significant positive correlation was demonstrated between the duration of a REMP episode and the succeeding non REMP sleep interval. The monkey patterns were quite similar to those of man.